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10.1177/1470320314543910 http://scihub22266oqcxt.onion/10.1177/1470320314543910 C4412792!4412792 !25143333     free     free     free Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\25143333 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       J+Renin+Angiotensin+Aldosterone+Syst 2015 ; 16 (2 ): 234-48 Nephropedia Template TP {{tp|p=25143333 |t=2015. ACE-inhibition increases podocyte number in experimental glomerular disease independent of proliferation |pdf=|usr=}}{{25143333 }} gab.com Text ACE-inhibition increases podocyte number in experimental glomerular disease independent of proliferation JO: J Renin Angiotensin Aldosterone Syst http://www.kidney.de/pget.php?&tw=1&pmid=25143333 #FOAvip OBJECTIVE: The objective of this article is to test the effects of angiotensin-converting enzyme (ACE)-inhibition on glomerular epithelial cell number in an inducible experimental model of focal segmental glomerulosclerosis (FSGS). BACKGROUND: Although ACE-inhibition has been shown to limit podocyte loss by enhancing survival, little is known about its effect on podocyte number following an abrupt decline in disease. METHODS: Experimental FSGS was induced with cytotoxic antipodocyte antibody. Following induction, groups were randomized to receive the ACE-inhibitor enalapril, the smooth muscle relaxant hydralazine (blood pressure control) or drinking water. Blood pressure, kidney function and histology were measured seven and 14 days following disease induction. RESULTS: Both glomerulosclerosis and urinary albumin-to-creatinine ratio were less in the ACE-inhibition arm at day 14. At day 7 of disease, mean podocyte numbers were 26% and 29% lower in the enalapril and hydralazine arms, respectively, compared to normal mice in which no antibody was injected. At day 14, the mean podocyte number was only 18% lower in the enalapril arm, but was 39% lower in the hydralazine arm compared to normal mice. Podocyte proliferation did not occur at any time in any group. Compared to water- or hydralazine-treated mice with FSGS, the enalapril arm had a higher mean number of glomerular parietal epithelial cells that co-expressed the podocyte proteins WT-1 and synaptopodin, as well as phospho-ERK. CONCLUSION: The results show following an abrupt decline in podocyte number, the initiation of ACE-inhibition but not hydralazine, was accompanied by higher podocyte number in the absence of proliferation. This was accompanied by a higher number of parietal epithelial cells that co-express podocyte proteins. Increasing podocyte number appears to be accompanied by reduced glomerulosclerosis. Twit Text FOAVip ACE-inhibition increases podocyte number in experimental glomerular disease independent of proliferation ????J Renin Angiotensin Aldosterone Syst http://www.kidney.de/pget.php?&tw=1&pmid=25143333 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25143333 #FOAvip English Wikipedia <ref>{{Cite pmid|25143333 }}</ref> ACE-inhibition increases podocyte number in experimental glomerular disease independent of proliferation #MMPMID25143333 Zhang J ; Yanez D ; Floege A ; Lichtnekert J ; Krofft RD ; Liu ZH ; Pippin JW ; Shankland SJ J Renin Angiotensin Aldosterone Syst 2015[Jun]; 16 (2 ): 234-48 PMID25143333 show ga OBJECTIVE: The objective of this article is to test the effects of angiotensin-converting enzyme (ACE)-inhibition on glomerular epithelial cell number in an inducible experimental model of focal segmental glomerulosclerosis (FSGS). BACKGROUND: Although ACE-inhibition has been shown to limit podocyte loss by enhancing survival, little is known about its effect on podocyte number following an abrupt decline in disease. METHODS: Experimental FSGS was induced with cytotoxic antipodocyte antibody. Following induction, groups were randomized to receive the ACE-inhibitor enalapril, the smooth muscle relaxant hydralazine (blood pressure control) or drinking water. Blood pressure, kidney function and histology were measured seven and 14 days following disease induction. RESULTS: Both glomerulosclerosis and urinary albumin-to-creatinine ratio were less in the ACE-inhibition arm at day 14. At day 7 of disease, mean podocyte numbers were 26% and 29% lower in the enalapril and hydralazine arms, respectively, compared to normal mice in which no antibody was injected. At day 14, the mean podocyte number was only 18% lower in the enalapril arm, but was 39% lower in the hydralazine arm compared to normal mice. Podocyte proliferation did not occur at any time in any group. Compared to water- or hydralazine-treated mice with FSGS, the enalapril arm had a higher mean number of glomerular parietal epithelial cells that co-expressed the podocyte proteins WT-1 and synaptopodin, as well as phospho-ERK. CONCLUSION: The results show following an abrupt decline in podocyte number, the initiation of ACE-inhibition but not hydralazine, was accompanied by higher podocyte number in the absence of proliferation. This was accompanied by a higher number of parietal epithelial cells that co-express podocyte proteins. Increasing podocyte number appears to be accompanied by reduced glomerulosclerosis. |Angiotensin-Converting Enzyme Inhibitors/pharmacology/*therapeutic use [MESH] |Animals [MESH] |Antibodies/metabolism [MESH] |Blood Pressure/drug effects [MESH] |Cell Count [MESH] |Cell Proliferation/drug effects [MESH] |Enalapril/pharmacology/therapeutic use [MESH] |Endpoint Determination [MESH] |Epithelial Cells/drug effects/metabolism/pathology [MESH] |Extracellular Signal-Regulated MAP Kinases/metabolism [MESH] |Glomerulosclerosis, Focal Segmental/chemically induced/*drug therapy/*pathology/physiopathology [MESH] |Mice [MESH] |Microfilament Proteins/metabolism [MESH] |PAX2 Transcription Factor/metabolism [MESH] |Phosphorylation/drug effects [MESH] |Podocytes/drug effects/enzymology/*pathology [MESH] |Protein Binding/drug effects [MESH] |Repressor Proteins/metabolism [MESH] |Systole/drug effects [MESH]ACE-inhibition increases podocyte number in experimental glomerular di(epmc).pdf DeepDyve Pubget Overpricing